1. www.advanceweb.com/NPPA • NURSE PRACTITIONER PERSPECTIVE • AUGUST 2016 13
Gastroenterology
GASTROESOPHAGEAL reflux disease (GERD) is one of
the most common gastrointestinal conditions in the United
States.1-4
The economic burden of GERD is estimated at more
than $24 billion annually.2
In addition to economic costs and
lost productivity, GERD significantly lowers quality of life.
More alarming, GERD is the most common predisposing
factor for esophageal adenocarcinoma.3
Heartburn and reflux
are the most typical symptoms of GERD, but many other
symptoms prompt inclusion of GERD in the differential list.4
Pathophysiology
Some degree of gastric content reflux is normal. GERD occurs
when the level of reflux causes symptoms and/or esophageal
mucosal injury. This abnormal amount of reflux is caused by
disruption of the antireflux barrier at the gastroesophageal
junction. The three primary mechanisms of gastroesophageal
junction incompetence are: transient lower esophageal sphincter
relaxations,ahypotensiveloweresophageal
sphincter, and anatomic disruption of the
gastroesophageal junction.5
Factors such
as hiatal hernia, obesity, delayed gastric
motility, supine position, alcohol, nicotine,
and certain foods can exacerbate gastro-
esophageal junction incompetence.3,5,6
Endogenous defenses protect against
gastric content, including pepsin and bile
products.3
Some of the defense mecha-
nisms include esophageal peristalsis,
saliva secretion and epithelial defenses. As
the assault on the esophagus continues,
the defenses become less effective. The
defenses are further reduced by factors
such as smoking, which decreases the
amount of saliva produced.
WhileGERDisaconditionofreflux,not
all reflux is acidic. In addition to typical
erosive reflux disease, manifestations such
as nonerosive esophageal reflux disease
(NERD)andextraesophagealrefluxdisease
exist and can include specific conditions
such as laryngopharyngeal reflux.7,8
Each
type of manifestation can have specific
symptoms and different etiologies.
In any manifestation of GERD in which
erosive content is refluxed, concern exists
for morphologic changes. As the esopha-
gus and upper airway continue to be
exposed to acidic fluids and their defen-
sive mechanisms weaken, they undergo
metaplastic changes. If exposure contin-
ues, the cells undergo dysplastic changes
and eventually advance to carcinoma.9
Diagnosis
Typical symptoms of GERD are heart-
burn (usually postprandial) and regurgi-
tation.1,4,6,10,11
Atypical symptoms include
epigastric fullness or pressure, epigastric
pain,dyspepsia,nausea,bloating,belching,
chronic cough, hoarseness, globus, chest
pain, chronic aspiration, bronchitis, sinus-
itis, dental erosion, sleep apnea, and water
brash.1,6,10,11
Alarm symptoms include dys-
phagia,odynophagia,bleeding,weightloss,
anemia, early satiety, and vomiting.1,6,10,11
Diagnosis of GERD can be made based
on clinical symptoms alone. Aids in diag-
nosis include response to acid suppression
therapy and diagnostics such as upper
GERD
Beyond the burning basics
By Michael Lemp, MSN, RN, NP-C
THINKSTOCK/GETTYIMAGES
DiagnosisofGERD
canbemade
basedonclinical
symptomsalone.

2. endoscopy, esophageal reflux monitoring
(pH and impedance testing), and esopha-
geal manometry.1,3,4,6,10
Diagnosis should
be made in a graduated manner, first with
consideration of symptoms and then with
response to acid suppression therapy.
Upper endoscopy should be reserved
for patients with alarm symptoms, high
risk of complications, patients refractory
to proton pump inhibitor (PPI) therapy,
or longstanding uncontrolled GERD.1,4
Esophageal reflux monitoring should
be reserved for patients refractory to
PPI therapy.1,4
Esophageal manometry
should be reserved for complex cases or
preoperative evaluation.1,4
Treatment
Treatment goals are symptom reduction,
esophageal healing, recurrence preven-
tion and prevention of complications.
Methods of treatment include diet and
lifestyle modifications, medications and
surgical intervention. Complex patients
and patients with GERD that is refractory
to PPI treatment should be referred to a
gastroenterology practice.
Lifestyle and diet modification is the
most cost-effective and efficient long-
term treatment option for GERD.1,4,6,10,11
Lifestyle modifications include weight
loss; smoking cessation; elevating the
head of the bed; avoiding postprandial
recumbency; and avoiding potentiating
medications.1,4,6,10,11
Diet modification
consists of eliminating trigger foods,
eating smaller portions and eating more
frequently, and avoiding large meals.1-5,10,11
The most common triggers of GERD
symptoms are caffeine, chocolate, alco-
hol, citrus products, tomato products,
onion, garlic, carbonated beverages, pep-
permint, fatty and fried foods, and spicy
foods.1,4,6,10,11
Lifestyle and diet modifica-
tions may not eliminate symptoms, but
they can decrease the need for medica-
tions and invasive procedures.
Medications have long been the main-
stay of GERD management.1,3
The two
most common classes used are hista-
mine 2 receptor agonists (H2RAs) and
PPIs. H2RAs are effective at reducing
postprandial acid in comparison to ant-
acids.1,3
H2RAs can also be utilized for
on-demand treatment and control of
nocturnal symptoms.1,3
PPIs should be
used for esophageal healing, relapse pre-
vention, and for treatment of moderate
to severe symptoms.1,3
PPIs can be used
to control GERD symptoms, but they
show less efficacy than when used for
erosive esophagitis.1,3
Both H2RAs and
PPIs should be taken 30 to 60 minutes
before eating; 30 minutes is ideal.1,3,4,6,10,11
Other medications can be used alone
or as adjuvant treatments to help control
symptoms. Some options include algi-
nates (e.g. sodium alginate), protectants
(e.g. sucralfate) and antacids (e.g. calcium
carbonate). 1,3,4,6,10,11
While these drugs
do not reduce acid, they can be quite
effective in treating symptoms.
In challenging cases, certain medica-
tions are effective in managing symptoms
or concomitant complicating disease
processes. These medications include
bile acid agents, prokinetics, GABAb
agonists, tricyclic antidepressants, selec-
tive serotonin reuptake inhibitors, and
trazadone.1,3,4,6,10,11
Their use should be
reserved for prescribers familiar with
them, due to the complexities of care.
Two dominant schools of thought
exist about treatment. The first is to start
with minimal treatment and titrate up
to desired effect. The second is to start
with high-dose therapy, titrate down
until recurrence, then move back to the
last effective regimen. Regimen selection
should be made by considering the clinical
efficacy of the proposed regimen, cost of
treatment and likelihood of patient adher-
ence.11
After symptom control has been
gained and the esophagus has had time
to heal (8 to 12 weeks), the provider can
attempt to discontinue therapy.4,11
The
providershouldbeawarethatcontinuation
of some level of treatment may needed for
ongoing symptom management.
For long-term GERD patients or
patients with refractory symptoms, surgi-
cal intervention is an option. Procedures
include fundoplication, bariatric surgery,
LINX procedure, and radiofrequency
ablation.1,3,4,6,10,11
Although surgery can
be advantageous, it is only 52% effective
at 3 to 5 years postprocedure.11
A Duty to Prevent Damage
The healthcare provider has a duty to
ensure that damage from GERD is arrest-
ed and not allowed to progress, since it
can result in carcinoma. While an astute
practitioner will understand the nuances
of treating GERD, he or she will also
know when to refer for consultation.
References
1. Badillo R, Francis D. Diagnosis and treatment of
gastroesophageal reflux disease. World J Gastrointest
Pharmacol Ther. 2014;5(3):105-112.
2. Kubo A, et al. Dietary guideline adherence for
gastroesophageal reflux disease. BMC Gastroenterol.
2014;14:144.
3. Nwokediuko SC. Current trends in the manage-
ment of gastroesophageal reflux disease: a review.
ISRN Gastroenterol. 2012;2012:391-631.
4. Katz PO, et al. Guidelines for the diagnosis and
management of gastroesophageal reflux disease. Am
J Gastroenterol. 2013;108(3):308-328.
5. Kahrilas PJ. Pathophysiology of reflux esopha-
gitis. UpToDate. http://www.uptodate.com/contents/
pathophysiology-of-reflux-esophagitis
6. Singhal V, Khaitan L. Gastroesophageal reflux
disease: diagnosis and patient selection. Indian J Surg.
2014;76(6):453-460.
7. Asaoka D, et al. Current perspectives on reflux
laryngitis. Clin J Gastroenterol. 2014;7(6):471-475.
8. Fisichella PM. Hoarseness and laryngopharyngeal
reflux. JAMA. 2015;313(18):1853-1854.
9. Oden KL. When heartburn gets serious: an
update on Barrett’s esophagus. ADVANCE for NPs &
PAs. 2011;2(8):37-38, 41, 50.
10. Kahrilas PJ. Clinical manifestations and diagnosis
of gastroesophageal reflux in adults. UpToDate. http://
www.uptodate.com/contents/clinical-manifestations-
and-diagnosis-of-gastroesophageal-reflux-in-adults
11. University of Michigan Health System.
Gastroesophageal Reflux Disease. http://www.med.
umich.edu/1info/FHP/practiceguides/gerd/gerd.12.pdf
MichaelLempisanursepractitioneratMetro
EastGastroenterologyinBelleville,Ill.
14 AUGUST 2016 • NURSE PRACTITIONER PERSPECTIVE • www.advanceweb.com/NPPA
Gastroenterology
Two schools of thought exist about treatment.
The first is to start with minimal treatment and
titrateuptodesiredeffect.Thesecondistostartwith
high-dose therapy, titrate down until recurrence,
then move back to the last effective regimen.